Expression data of cardiac and gastrocnemius muscles of tumor bearing C26 mouse
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE63032 | GEO | 2014/11/10
SECONDARY ACCESSION(S): PRJNA266482
REPOSITORIES: GEO
Similar Datasets
Project description:Cancer cachexia is a metabolic multifactorial syndrome that causes up to 20% of cancer-related deaths. Muscle atrophy, the hallmark of cancer cachexia, strongly impairs the quality of life of cancer patients; however, the underlying pathological process is still poorly understood. In our study, the transcriptome of cachectic gastrocnemius muscle in the C26 xenograft model was comparied with normal control. The key pathways involving this diseases was discovered according to the different expressed genes.
2021-05-27 | GSE175570 | GEO
Project description:Cachexia is an exacerbating event in many types of cancer that is strongly associated with a poor prognosis. We have identified cytokine, signaling and transcription factors that are required for cachexia in the mouse C26 colon carcinoma model of cancer. C2C12 myotubes treated with conditioned medium from C26 cancer cells induced atrophy and activated a STAT-dependent reporter gene but not reporter genes dependent on SMAD, FOXO, C/EBP, NF-ĸB, or AP-1. Of the gp130 family members IL-11, IL-6, oncostatin M (OSM), and leukemia inhibitory factor (LIF), only OSM and LIF were sufficient to activate the STAT reporter in myotubes. A LIF blocking antibody abolished C26 CM-induced STAT reporter activation STAT3 phosphorylation and myotube atrophy, but blocking antibodies to IL-6 or OSM did not. JAK2 inhibitors also blocked the C26 CM-induced STAT reporter activation, STAT3 phosphorylation, and atrophy in myotubes. LIF at levels found in the C26 CM was sufficient for STAT reporter activation and atrophy in myotubes. In vivo, an increase in serum LIF preceded the increase in IL-6 in mice with C26 tumors. Overexpression of a dominant negative Stat3Cβ-EGFP gene in myotubes and in mouse muscle blocked the atrophy caused by C26 CM or C26 tumors, respectively. Taken together these data support an important role of LIF- JAK2-STAT3 in C26 cachexia and point to a therapeutic approach for at least some types of cancer cachexia. from three replicate wells of cells at each treatment, pools of total RNA were used to create cDNA which were evaluated on Affymetrix mouse gene 1.0 ST v.1 arrays.
2015-06-25 | E-GEOD-68827 | biostudies-arrayexpress
Project description:Cachexia is an exacerbating event in many types of cancer that is strongly associated with a poor prognosis. We have identified cytokine, signaling and transcription factors that are required for cachexia in the mouse C26 colon carcinoma model of cancer. C2C12 myotubes treated with conditioned medium from C26 cancer cells induced atrophy and activated a STAT-dependent reporter gene but not reporter genes dependent on SMAD, FOXO, C/EBP, NF-ĸB, or AP-1. Of the gp130 family members IL-11, IL-6, oncostatin M (OSM), and leukemia inhibitory factor (LIF), only OSM and LIF were sufficient to activate the STAT reporter in myotubes. A LIF blocking antibody abolished C26 CM-induced STAT reporter activation STAT3 phosphorylation and myotube atrophy, but blocking antibodies to IL-6 or OSM did not. JAK2 inhibitors also blocked the C26 CM-induced STAT reporter activation, STAT3 phosphorylation, and atrophy in myotubes. LIF at levels found in the C26 CM was sufficient for STAT reporter activation and atrophy in myotubes. In vivo, an increase in serum LIF preceded the increase in IL-6 in mice with C26 tumors. Overexpression of a dominant negative Stat3Cβ-EGFP gene in myotubes and in mouse muscle blocked the atrophy caused by C26 CM or C26 tumors, respectively. Taken together these data support an important role of LIF- JAK2-STAT3 in C26 cachexia and point to a therapeutic approach for at least some types of cancer cachexia.
2015-06-25 | GSE68827 | GEO
Project description:Existing data suggest that NF-kappaB signaling is a key regulator of cancer-induced skeletal muscle wasting. However, identification of the components of this signaling pathway and of the NF-M-NM-:B transcription factors that regulate wasting is far from complete. In muscles of C26 tumor bearing mice, overexpression of d.n. IKKM-NM-2 blocked muscle wasting by 69%, the IM-NM-:BM-NM-1-super repressor blocked wasting by 41%. In contrast, overexpression of d.n. IKKM-NM-1 or d.n. NIK did not block C26-induced wasting. Surprisingly, overexpression of d.n. p65 or d.n. c-Rel did not significantly block muscle wasting. Genome-wide mRNA expression arrays showed upregulation of many genes previously implicated in muscle atrophy. To test if these upregulated genes were direct targets of NF-M-NM-:B transcription factors, we compared genome-wide p65 or p50 binding to DNA in control and cachectic muscle using ChIP-sequencing. Bioinformatic analysis of ChIP-seq data from control and C26 muscles showed increased p65 and p50 binding to a few regulatory and structural genes but only two of these genes were upregulated with atrophy. The p65 and p50 ChIP-seq data are consistent with our finding of no significant change in protein binding to an NF-M-NM-:B oligo in a gel shift assay. Taken together, these data support the idea that although inhibition of IM-NM-:BM-NM-1, and particularly IKKM-NM-2, blocks cancer-induced wasting, the alternative NF-M-NM-:B signaling pathway is not required. In addition, the downstream NF-M-NM-:B transcription factors do not regulate the transcriptional changes. These data are consistent with the growing body of literature showing that there are NF-M-NM-:B-independent substrates of IKKM-NM-2 and IM-NM-:BM-NM-1 that regulate physiological processes. To compare gene expression changes in atrophied muscles from C26 tumor bearing mice, gastrocnemius/plantaris muscles were harvested from 4 C26 tumor-bearing mice, and 3 control non tumor-bearing mice. Total RNA were isolated and pooled (2-3 muslces in the same group per RNA sample ) to make equal amount of total RNA per sample. Three pooled total RNA samples from healthy control muscles and 3 pooled total RNA from muscles of C26 tumor bearing mice were labelled and hybridized on 6 Mouse Affyemtrix Gene 1.0 ST arrays. Two-side t-tests and multiple test corrections were performed to identify differentially expressed genes due to C26 tumor bearing induced cachexia.
2013-11-15 | E-GEOD-48363 | biostudies-arrayexpress
Project description:Background The prevailing view is that a combination of nutritional, pharmacological and exercise therapy is most optimal to reduce the development and progression of cancer cachexia. However, in many cancer patients, physical activity is hampered by frailty and fatigue. The present study aimed to investigate whole-body vibration training (WBV) as potential alternative to attenuate loss of weight, muscle mass and function in tumour bearing mice. Methods Twenty-four male CD2F1-mice (21.5±0.2g) were stratified into four groups (control=[C], control+WBV=[C+V], tumour-bearing=[T] and tumour-bearing+WBV=[T+V]), and injected (day 1) with C26 cells or vehicle. From day 1, whole-body-vibration (WBV groups) was performed for 19 days (15min, 45Hz, 1.0g acceleration). General outcome measures included body mass and composition, and daily activity. In addition, blood analysis and assessments of muscle histology and function and whole genome gene expression in m. soleus (SOL) and m. extensor digitorum longus (EDL) were performed. Two-way ANOVA with factors tumour, training and interaction was used for statistical analysis. Results Body weight, lean and fat mass and EDL mass were all lower in tumour bearing mice compared to controls. No effects of vibration training were found on systemic cachexia related outcomes. However, WBV increased EDL mass in the control treatment,. SOL mass did not differ, whereas SOL function was affected by both tumour and WBV. Interestingly, WBV reduced the tumour-related effects on muscle gene expression in EDL, SOL and heart. Conclusions These data suggest that WBV had only minor effects on cachexia related outcomes in the present experimental set-up, while muscle transcriptome was positively affected. This merits follow-up studies applying for example longer treatment periods or incorporating WBV in a multiple-target intervention.
2020-11-01 | GSE121972 | GEO
Project description:Analysis of gene expression in CD2F1 mice with cancer cachexia due to implantation of C26 colon carcinoma cells. Total RNA obtained from quadriceps muscle of female CD2F1 mice with early weight loss (10%) or severe weight loss (15%) due to intrascapular subcutaneous implantation of one million C26 colon adenocarcinoma cells.
2011-08-29 | E-GEOD-24112 | biostudies-arrayexpress
Project description:Next Generation Sequencing of mRNA of cachectic mice muscles in C26 model
| PRJNA732917 | ENA
Project description:RNA sequencing of white adipose, brown adipose tissue and gastrocnemius muscle isolated from non-tumor bearing and HT1080 tumor-bearing mice treated with control IgG1 or anti-GFRAL 3P10
2020-07-20 | GSE149263 | GEO
Project description:Expression data of cardiac and gastrocnemius muscles of tumor bearing C26 mouse
| PRJNA266482 | ENA
Project description:Analysis of gene expression in CD2F1 mice with cancer cachexia due to implantation of C26 colon carcinoma cells.
2011-08-30 | GSE24112 | GEO